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Ascorbic acid has been considered, for a long time, only as an antioxidant. Since a few years, growing evidences, from literature, demonstrate that this molecule has other function. This is why different groups tried to find new targets for ascorbic acid, not only to prevent scurvy, but also as a drug. In this line of evidence, we report that high doses of ascorbic acid partially correct the phenotype of a Charcot–Marie–Tooth type 1A model, created in the lab. Based on this result, several clinical trials have been undertaken. Unfortunately, they have been controversial, primary outcomes never been reached, but tendencies observed. What conclusion could we draw? This will be discussed below. We published, in 2004, an article demonstrating that treatment of an animal model of CMT1A by high dose of ascorbic acid (AA), partially restores myelination and normal locomotion [1] . Our research was based on articles demonstrating that AA is necessary for myelination in co-culture of axon and Schwann cells [2] , [3] , [4] . This article was followed by clinical trials. Visioli et al. [5] recently published, in this journal, an article discussing AA treatment in Charcot–Marie–Tooth [5] . In this publication they use pharmacokinetics arguments to affirm that ascorbic acid could not be a treatment for CMT1A. In this paper, we will present arguments that demonstrate that this conclusion could be commented, as numerous arguments, based on literature, are not present in the article. We will thus expose these additional arguments, in the following sections. |
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